All-trans-Retinoic Acid Attenuates Radiation-Induced Intestinal Fibrosis in Mice

Okoshi, Kae; Kubo, Hajime; Nagayama, Satoshi; Tabata, Chiharu; Kadokawa, Yoshio; Hisamori, Shigeo; Yonenaga, Yoshikuni; Fujimoto, Akihisa; Mori, Akira; Onodera, Hisashi; Watanabe, Go; Sakai, Yoshiharu

doi:10.1016/j.jss.2007.12.762

Cited by 10 publications

(9 citation statements)

References 23 publications

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“…Yeh et al 36 showed that 10 Gy whole‐body irradiation caused chronic intestinal fibrosis after irradiation. Linard et al 23 and Okoshi et al 24 established a murine model of late radiation‐induced intestinal fibrosis with 10 and 15 Gy abdominal irradiation, respectively. In the current study, we established an intestinal fibrosis model after a single dose of 10 Gy abdominal irradiation.…”

Section: Discussionmentioning

confidence: 99%

“…Terminal ileum was fixed in 4% buffered paraformaldehyde and embedded in paraffin. Sections (5 µm) were stained with hematoxylin and eosin (H&E) to evaluate histological changes and Masson's trichrome staining (MTS) to assess the severity of collagen deposition as previously reported 24 . The thickness of the submucosa was evaluated randomly in 5 fields in every sample.…”

Section: Methodsmentioning

confidence: 99%

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Soluble Dietary Fiber Ameliorates Radiation‐Induced Intestinal Epithelial‐to‐Mesenchymal Transition and Fibrosis

Yang

Ding

Dai

et al. 2016

J Parenter Enteral Nutr

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Soluble Dietary Fiber Ameliorates Radiation‐Induced Intestinal Epithelial‐to‐Mesenchymal Transition and Fibrosis

Yang

Ding

Dai

et al. 2016

J Parenter Enteral Nutr

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“…Okoshi et al ’s [51] research shows that administration of ATRA attenuated irradiation-induced intestinal fibrosis and concomitantly reduced the expression of IL-6 and TGF-β1. They could determine from further in vitro studies that ATRA suppressed the trans-differentiation of irradiated intestinal fibroblasts and reduced the production of α-SMA and collagen.…”

Section: Role Of Ra In Diseasesmentioning

confidence: 99%

The Controversial Role of Retinoic Acid in Fibrotic Diseases: Analysis of Involved Signaling Pathways

Zhou

Drummen²,

Qin

2012

IJMS

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Fibrotic diseases, such as liver, pulmonary and renal fibrosis, are common end-stage conditions and represent a major global health problem. Furthermore, effective therapeutic measures are presently unavailable. Extracellular matrix accumulation is the most prominent characteristic in the pathogenesis of fibrotic disease. Retinoic acid, including all-trans retinoic acid, 9-cis and 13-cis retinoic acid, play important roles in various physiological processes, such as in embryonic development, reproduction, vision, cell growth, differentiation, apoptosis and inflammation. Present studies report that retinoic acid treatment may affect various processes involved in the onset and progression of fibrotic disease. However, the therapeutic effects of retinoic acid in such diseases remain controversial. Several reports indicate that retinoic acid positively affects the progression of fibrosis and alleviates the accumulation of the extracellular matrix, whereas other studies report the opposite; that retinoic acid exacerbates fibrosis and induces extracellular matrix accumulation. Signaling pathways might be an important influencing factor and differences in signaling events might be responsible for the contradictory role of retinoic acid in fibrotic diseases. Since there was no review available that investigated the role of retinoic acid and the signaling pathways involved, we retrospectively studied the literature and provide a comprehensive analysis of retinoic acid’s role in fibrotic diseases, and provide an overview of the signal transduction pathways involved in its pathogenesis.

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“…Radiation-induced intestinal disease has also been successfully modeled in mice (Followill et al, 1993; Okoshi et al, 2008) permitting informative strain variation investigations and the evaluation of genetic modifications on trait development. Firstly, important investigations in a mouse model have revealed dose dependent responses to develop in the intestines of C3Hf/Kam mice wherein the extent of early crypt depletion dictated the risk of obstruction (Followill et al, 1993).…”

Section: Post-irradiation Tissue Repairmentioning

confidence: 99%

Mouse genetic approaches applied to the normal tissue radiation response

Haston¹

2012

Front. Oncol.

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The varying responses of inbred mouse models to radiation exposure present a unique opportunity to dissect the genetic basis of radiation sensitivity and tissue injury. Such studies are complementary to human association studies as they permit both the analysis of clinical features of disease, and of specific variants associated with its presentation, in a controlled environment. Herein I review how animal models are studied to identify specific genetic variants influencing predisposition to radiation-induced traits. Among these radiation-induced responses are documented strain differences in repair of DNA damage and in extent of tissue injury (in the lung, skin, and intestine) which form the base for genetic investigations. For example, radiation-induced DNA damage is consistently greater in tissues from BALB/cJ mice, than the levels in C57BL/6J mice, suggesting there may be an inherent DNA damage level per strain. Regarding tissue injury, strain specific inflammatory and fibrotic phenotypes have been documented for principally, C57BL/6 C3H and A/J mice but a correlation among responses such that knowledge of the radiation injury in one tissue informs of the response in another is not evident. Strategies to identify genetic differences contributing to a trait based on inbred strain differences, which include linkage analysis and the evaluation of recombinant congenic (RC) strains, are presented, with a focus on the lung response to irradiation which is the only radiation-induced tissue injury mapped to date. Such approaches are needed to reveal genetic differences in susceptibility to radiation injury, and also to provide a context for the effects of specific genetic variation uncovered in anticipated clinical association studies. In summary, mouse models can be studied to uncover heritable variation predisposing to specific radiation responses, and such variations may point to pathways of importance to phenotype development in the clinic.

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All-trans-Retinoic Acid Attenuates Radiation-Induced Intestinal Fibrosis in Mice

Abstract: Our findings indicate that ATRA ameliorates irradiation-induced intestinal fibrosis. ATRA could be a novel approach in the treatment of fibrosis associated with chronic radiation enteritis.

Cited by 10 publications

References 23 publications

Soluble Dietary Fiber Ameliorates Radiation‐Induced Intestinal Epithelial‐to‐Mesenchymal Transition and Fibrosis

Soluble Dietary Fiber Ameliorates Radiation‐Induced Intestinal Epithelial‐to‐Mesenchymal Transition and Fibrosis

The Controversial Role of Retinoic Acid in Fibrotic Diseases: Analysis of Involved Signaling Pathways

Mouse genetic approaches applied to the normal tissue radiation response

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